Veterinary Surgery, 20, 5, 282-290, 1991
Healing Characteristics of Free and Pedicle Fat Grafts after Dorsal Laminectomy and Durotomy in Dogs
Dorsal laminectomy and durotomy were performed at thoracic vertebrae 12 and 13 (T12-Tl3) and lumbar vertebrae 1 and 2 (Ll-L2) in 12 normal dogs. A free fat graft harvested from subcutaneous tissue adjacent to the incision was placed over the T12-T13 laminectomy site. A 75 X 25 x 5 mm pedicle fat graft harvestedfrom a similar location was placed over the LlL2 laminectomy site. Three dogs each were euthanatized at weeks 2, 4, 8, and 16. With both types of fat grafts, an initial inflammatory stage reduced the size of the graft approximately 50%. Axonal degeneration and demyelination of the spinal cord resolved by week 16. At week 16, the durotomy sites had healed, but the dura mater was adhered to the spinal cord. No difference between the grafts could be demonstrated by antemortern myelography and cerebrospinal fluid analysis. There was no demonstrable advantage to the use of pedicle fat grafts.
of a laminectomy is T formation of an epidural scar referred to as a laminectomy membrane. Excessive perineural fibrosis and HE INEVITABLECONSEQUENCE
scamng, dural adhesions, nerve root attenuation, and spinal cord compression and degeneration may complicate the healing process. The scar tissue may complicate surgical re-exploration of the laminectomy site. Nevertheless, such scar tissue formation is infrequently recognized as a clinical problem. Clinical manifestations of such complications are especially rare after heniilaminectomy; when present, they are usually associated with dorsal laminectomy procedures.I Many investigators have attempted to modify or to prevent formation of this scar tissue to avoid potential complications. Methods include modifications of surgical technique, pharmacologic manipulation of the healing process, and implantation of biologic and nonbiologic materials to separate the dura To from the raw surface of the paraspinal date, the most success appears to have been achieved with implantation of autogenous fat, either as a free fat graft or as a pedicle fat graft. It has been suggested that pedicle
grafts are superior to free grafts in preventing dural scar formation and bone closure over the laminectomy site and in protecting the spinal cord.24 The purpose of this investigation is to compare the healing characteristics of free and pedicle fat grafts placed over laminectomy and durotomy sites in dogs. Materials and Methods Two noncontiguous modified dorsal laminectomies (complete excision of the dorsal lamina and caudal articular processes, with excavation of the lateral laminae and pedicles) were performed in 12 mature, preconditioned beagle dogs.’ One laminectomy was centered over the junction of thoracic vertebrae 12 and 13 (T12-T 13) and one was centered over the junction of lumbar vertebrae I and 2 (Ll-L2). At each laminectomy site, a dorsal midline durotomy was performed. A free fat graft was harvested from the subcutaneous tissue dorsal to the deep fascia overlying the epaxial muscles and adjacent to the incision. Each graft was 5 to 7 mm thick, and each was
From the Departments of Small Animal Clinical Sciences (Trevor, Martin) and Pathobiology (Saunders), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, and the Department of Clinical Sciences (Trotter), New York State College of Veterinary Medicine, Ithaca, New York. Presented at the 20th Annual Meeting of the American College of Veterinary Surgeons, San Diego, California, February 1985. No reprints available.
282
TREVOR, MARTIN, SAUNDERS, AND TROTTER
283
Fig. 1. Fat grafts with dorsal laminectomy, week 2. Connective tissue septae are visible as narrow bands of white tissue coursing through the grafts. Distortion of the spinal cord is evident. Arrowheads delineate the fat grafts. (A) Free fat graft. (B)Pedicle fat graft.
trimmed to fill the bony defect created by the T I2-T 1 3 laminectom y. Pedicle fat grafts were created by sharply detaching subcutaneous fat along the margin of the incision, leaving the base attached caudally. The grafts were approximately 25 mm wide, 75 mm long, and 5 mm thick, with the length approximately three times the width of the base. The graft was placed directly over the spinal cord at the LI-L2 laminectomy site. In an attempt to avoid vascular compromise, the epaxial fascia adjacent to penetration of the pedicle graft was not closed. Mependine HCl (2.24.4 mg/kg) was administered as necessary to control postoperative pain. Three dogs each were euthanatized at weeks 2, 4, 8, and 16. Immediately before euthanasia, cerebrospinal fluid was collected by cisternal tap for Pandy test, cytologic evaluation including total and differential cell counts, and measurement of glucose, protein, pH, and specific gravity. Lumbar myelography was performed at the L4-L5 interspace. After necropsy, the vertebral column was removed intact from T10 to L4, dissected free of muscle, and frozen. While still frozen, transverse sections 1 cm thick were made with a band saw. The sections through disc spaces T11-Tl2, T12-Tl3, T13-L1, Ll-L2, and L2-L3 were thawed, fixed in 10% neutral buffered formalin, and decalcified. Prepared sections were stained with H & E and Masson’s tnchrome for collagen.
Results Eight dogs were nonambulatory (unable to support weight or walk with the hind limbs) immediately or within the first 72 hours after surgery. Four dogs remained ambulatory (capable of bearing weight and walking unassisted with hind limbs), but three were ataxic or had conscious propnoceptive deficits. All dogs euthanatized at weeks 2 and 4 were nonambulatory with diminished or no deep pain. At week 8, the six remaining dogs were walking, one with mild pelvic limb ataxia. The three dogs remaining at week 16 were walking normally. The results of the cerebrospinal fluid examinations were normal for all 12 dogs. Myelographic evidence of mild to severe spinal cord swelling, seen as vaned narrowing of the contrast columns, was present under six pedicle grafts and eight free grafts. Dorsal cord compression, identified by ventral deviation of the dorsal contrast column, was present under two pedicle grafts and two free grafts. Widening of the dorsal contrast column was present under one pedicle graft and one free graft. There was no consistent correlation between the nature or seventy of myelographic changes and the type of fat graft used to fill the laminectomy defect. At necropsy, pronounced dorsoventral compression of the spinal cord by both types of fat grafts was evident at week 2. At week 4, similar though less severe compression
FAT GRAFTS AFTER LAMINECTOMY
Fig. 2. Fat grafts with dorsal laminectomy, week 4. The fat is inflamed, with a mottled grey-and-white appearance. Arrowheads delineate the fat grafts. (A) Free fat graft. (B) Pedicle fat graft.
was evident. By week 8, the spinal cord had regained a more normal cross-sectional appearance, and at week 16 the shape of the spinal cord was normal. Grafts in both sites had shrunk 25% to 50% at week 2, and 50%by week 8. At week 16, each graft was about one-half its original thickness. Grey-white fat was identifiable, and fibrosis was evident as narrow bands of distinct white tissue coursing through the grafts. Foci of fat resorption and inflammation were visible as areas of yellow-brown discoloration within the grafts (Figs. 1-4). Histologically, inflammation, fat cell degeneration, and fibrosis were moderately severe at week 2. The inflammatory cell infiltrate consisted mainly of macrophages, lymphocytes, and plasma cells, with some scattered neutrophils. The neutrophils disappeared by week 4, by which time the fat degeneration and fibrosiswere more extensive. Associated with fat cell degeneration was formation of locules of free fat that appeared to induce a granulomatous response, including the formation of multinucleate giant cells. Severe inflammation, fat resorption, and fibrous tissue proliferation reached a peak in both grafts at week 8, and resolution of the inflammatory process and fat degeneration began (Fig. 5). In one dog euthanatized at week 8, there was only minimal inflammation in each graft. In two dogs, there was severe inflammation in the free fat
graft, but only mild change in the pedicle fat graft. By week 16, all inflammatory and degenerative changes had subsided in both grafts, leaving viable fat cells and a few delicate connective tissue septa (Fig 6). Significant inflammation was also evident adjacent to the grafts. At week 2, in the area previously occupied by the dorsal arch, numerous fragments of bone and suture were surrounded by a granulomatous response. This reaction subsided considerably by week 4, and was only occasionally present at week 8. The gap created in the dura mater filled in with fibrous connective tissue by week 2. In some locations involving both graft sites, this fibrosis was quite extensive and adhered to the dorsal surface of the spinal cord (Fig 7). The spinal cord at both graft sites suffered extensive axonal swelling and demyelination of all funiculi at week 2 (Fig. 8). Only mild changes were evident at week 4, and by week 8 they were nearly absent. No spinal cord abnormalities were present at week 16, but the dura mater, though rejoined, was still adherent to the spinal cord.
Discussion A multifactorial etiology has been proposed for laminectomy membrane formation, including factors such as
285
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 3. Fat grafts with dorsal laminectomy, week 8. Fat is visible. Spinal cord shows less distortion when compared with the 2-week group. Arrowheads delineate the fat grafts. (A) Free fat graft. (B) Pedicle fat graft.
length and location of the laminectomy site, hemostasis, height of remaining laminar bone, extent of epidural fat removal, and the type of implant interposed between the dura mater and paraspinal muscles.6 Laminectomy defects heal in a manner resembling endochondral bone formation arrested as a fibrous nonunion. Organization of the hematoma is followed by fibroblast invasion from the overlying epaxial muscles, resulting in fibrous callus formation and subsequent metaplasia to cartilage and sometimes b ~ n e . ~ Sequelae ,~.' include excessive cicatrix formation and epidural fibrosis, spinal dural scarring and adhesions, nerve root attenuation and entrapment, degeneration of the spinal cord, and stenosis of the spinal anal.^.^,' The scar tissue that forms may complicate re-exploration of the pine.^.^ Clinical manifestations of such complications, however, are infrequent. In a retrospective study of 187 dogs that underwent dorsal laminectomy and facetectomy, laminectomy membrane was a complication in only three dogs.* Modifications of surgical technique have been described, with smaller laminectomy defects and careful attention to hem0stasis.6,~In general, performing hemilaminectomies instead of laminectomies whenever possible has resulted in a lower incidence of clinical laminectomy membrane complications.I Nevertheless, dorsal laminectomy is preferred by some surgegns, especially for ventrally-situated disc herniations or when lateralization of
cord compression is not evident clinically or myelographically.',' Pharmacologic modification of the healing process with locally and parenterally administered pharmaceutic agents, including corticosteroids and hyaluronic acid, has been tried without S U C C ~ S S . ~ ~ ~ ~ ~ ~ - ' ~ Perhaps the best results have been achieved by interposing material to separate the spinal cord and dura mater from damaged paraspinal muscles. Nonbiologic materials that have been interposed include absorbable gelatin sponge, oxidized regenerated cellulose, absorbable gelatin film, micropore tape, methyl methacrylate, dacron, mylar, dimethyl siloxane polymer, polyethylene and other acrylic plastics, and polyglactin 9 R esults with these materials have been extremely varied and often less than optimal. Newer materials such as polylactic acid membrane and Elastase* have shown more p r o m i ~ e . ' ~ . ' ~ Biologic implants have also been investigated. k e l bone graft (contoured bovine bone) was found to be of some benefit in preventing invasion of scar tissue into the spinal canal." Porcine dermis treated to reduce its antigenic properties? did not prevent adhesions from forming after spinal surgery in rabbits." Autogenous fat grafts form an effective barrier, limiting scar extension into the spinal canal, decreasing scar tissue formation, and preventing 13'3-15
* Eisai Co. Ltd., Tokyo, Japan. t Zenoderm. Ethicon Ltd., Edinburgh. Scotland.
FAT GRAFTS AFTER LAMINECTOMY
Fig. 4. Fat grafts with dorsal laminectomy,week 16. Fat is normal in appearance, although reduced in size. No evidence of scar invasion into the spinal canal. In figure 4B, the pedicle of the fat graft is visible. Arrowheads delineate the fat grafts. (A) Free fat graft. (8)Pedicle fat graft.
dural adhesion^.^^'^^'^^^^ It has been suggested that the fat graft occupies a space that otherwise would become filled by hematoma.8Because it is flexible, the fat graft conforms to the margins of the laminectomy site, preventing leaks along which scar tissue might invade. Fat grafts avoid complications associated with stiffer nonbiologic materials, specifically problems with marginal fitting, implant displacement, and alteration of spinal biomechanics.6Fat grafts also reportedly avoid problems associated with flexible membranous nonbiologic materials, such as depression of the implant against the cord and subsequent dorsoventral flattening of the spinal canal.6 In this study, however, both free and pedicle fat grafts were responsible for severe dorsoventral cord compression that was apparent at week 2 and still evident at week 4.The neurologic status of these animals (nonambulatory paraparesis) and the histologic appearance of the spinal cord (axonal swelling and demyelination) were compatible with a compressive lesion. The cord compression may have been caused by the size (bulk) of the graft, postoperative inflammation and swelling of the fat graft, or closure of the epaxial fascia. Similar complications have been reported in Neurologic morbidity may have been higher in the dogs in this study than in clinical patients because the spine was destabilized by dorsal laminectomy in two locations rather than one, as is common in the clinical situation.26Nevertheless, it has been established that fat grafts are acceptable in clinical patients. It has
also been established that durotomy causes increased neurologic m~rbidity.~’ Reduction of the cord compression by weeks 8 and 16 probably resulted from resolution of the initial inflammation and swelling of the fat graft, decrease in the size of the fat graft by necrosis, and maturation of the granulation tissue into a more rigid connective tissue framework able to maintain cord shape. Although almost all remaining dogs in this study were clinically normal by weeks 8 and 16, care has to be taken to avoid compression of the spinal cord by the fat graft. In clinical patients, the symptoms of such compression may be confused with the symptoms of the transverse myelopathy for which the laminectomy procedure was performed. It has been recommended that a loop of 20or 22-gauge orthopedic wire be used to span the laminectomy defect. The wire is placed around the rostra1 and caudal spinal processes and moderately tightened, and the fascia and epaxial muscles are then sutured over the wire.’ This may aid in retaining a more normal architecture in the region of the laminectomy defect. To avoid excessive bulk that might compress the dura mater or nerve roots, the fat graft should be just large enough to cover the laminectomy defect and no more than 3 to 5 mm thick. Althou@ clinical success has been reported with thicker implants (10-1 5 rnm),l4 other investigators have obtained better results with grafts no thicker than 3 mm.3 During closure of the epaxial fascia, care should be
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 5. Severely inflamed free fat graft, week 8. Dense connective tissue can be seen infiltratingthe fat graft, surrounding the remaining foci of fatty tissue. H & E; x15. EM = epaxial musculature; FG = fat graft; SC = spinal cord.
287
Fig. 6. Free fat graft, week 16. There is complete resolution of the inflammation with normal fat. H & E; x15. FG = fat graft; DM = dura mater; SC = spinal cord.
between caudally based and cranially based flaps, or betaken to avoid forcing the fat graft and epaxial muscutween flaps brought over the midline and flaps tunneled lature onto the exposed spinal cord. through the adjacent mu~culature.~ In this study, 5 mm After implantation, a free fat graft goes through an inithick caudally based pedicle flaps were brought over the tial process involving necrosis of fat cells. Death of pormidline, taking care to avoid compression and vascular tions of the graft results in fat cyst formation, giant cell compromise of the pedicle by leaving the epaxial fascia formation, cellular infiltration, and f i b r o s i ~ . ~ , ~This , ' ~ . ~ ' adjacent to graft penetration unsutured. results in shrinkage of the fat graft to approximately onePedicle fat grafts are reported to be superior to free half its original s i ~ e . ~ .The ' ~ , remaining '~ implant survives grafts in preventing closure of bone over the laminectomy because of revascularization through a local blood supsite by preventing metaplasia of scar tissue to cartilage ply.3,'2.'4,2'928 Survival of a free fat graft is influenced by and bone.3 Fat cells of the pedicle grafts have been shown the amount of blood lost during the surgical procedure, to have improved survival with less cellular infiltration and fewer areas of fat necro~is.~ Pedicle fat grafts are rethe extent of surgical dissection, and the thickness of the portedly more effective than free fat grafts in preventing fat graft itself." dural scar formation and protecting the spinal cord against Several investigators have found pedicle fat grafts to be fibrosis and degenerative change^.^,^ Presumably, the superior to free fat In dogs, the deep fat derives its blood supply mainly from the deep f a ~ c i aFlaps . ~ with blood supply entering the fat graft through the attached a length-to-width ratio of 3: 1 and a thickness not greater pedicle maintains the viability of the graft, yielding superior results. than 3 mm were recommended. There was no difference
200
FAT GRAFTS AFTER LAMINECTOMY
Fig. 7. Free fat graft, week 2. The margins of the durotomy incision have scarred together and adhered to the spinal cord beneath. H 8 E; x20. FG = fat graft; DM = dura mater; SC = spinal cord.
The results of this study, however, indicated that the processes of healing and scar tissue formation were similar in both grafts. Each progressed through a severe granulomatous inflammation in response to fat degeneration, resulting in fibrosis and shrinkage of the graft, with the most extensive and severe changes 8 weeks after implantation. By week 16, the inflammatory process had resolved, leaving a viable fat graft reduced approximately 50% in size. In some cases, this shrinkage had become apparent as early as week 2. By week 16, the dura had rejoined but was adherent to the spinal cord. Histologically, there was no difference in healing of the durotomy sites. Extensive axonal degeneration and demyelination of the spinal cord at week 2, with resolution by week 16, was a reflection of the degree of cord compression. Myelographically and by gross inspection, no difference in cord compression could be demonstrated between graft types. In this study, no difference in healing properties or in the final outcome could be demonstrated between free and pedicle fat grafts.
There are several possible explanations for the similar results with both types of grafts in this study. No vascular studies were performed to define blood supply to the pedicle graft. This study mimicked clinical situationsin which the pedicle is based on paraspinal fat adjacent to the dorsal laminectomy site, not on a particular “axial pattern artery.” The laminectomy sites (T 12-T 13 and L 1-L2) are equally common sites of intervertebral disc protrusions treated by laminectomy. It is possible that the pedicle graft did not maintain circulation immediately after transposition. Consequently, both types of grafts may have been avascular from the beginning and thus may have had similar healing characteristics. Alternatively, the pedicle may have maintained perfusion to the graft, but neovascularization of the free graft may have occurred rapidly enough that by week 2 it was essentially complete; hence, healing of the two types of grafts was similar. Subjectively, there was no obvious difference in the amount of collagen (demonstrated with Masson’s trichrome stain) between the two grafts, indicating a similar inflammatory response.
289
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 8. Free fat graft, week 2.There is axonal swelling and demyelination of the spinal cord. H 8 E; X75.
Since inflammation is a vascular event, this would imply similar vascularity. With either explanation, the similarity in healing indicates that there were no distinct advantages to the use of pedicle fat grafts in this study. Because of the ease and speed with which they can be harvested, our recommendation is to use free fat grafts with dorsal laminectomy. However, considerable care must be taken to avoid compression of the spinal cord by the fat graft. Furthermore, if adequate treatment can be provided by hemilaminectomy, then avoiding the dorsal laminectomy approach whenever possible is probably justified.
References I . Gage ED, Hoerlein BF. Hemilaminectomy and dorsal laminectorny for relieving compressions of the spinal cord in the dog. J Am Vet Med Assoc 1968;152:351-359. 2. Sakamoto K. Experimental study o n pedicle fat grafts after faminectomy: Comparison of pedicle fat and free fat grafts. Nippon Seikeigeka Gakkai Zasshi 1987;61:743-753. 3. Gill GG, Sakovich L, Thompson E. Pedicle fat grafts for the prevention of scar formation after laminectomy: An experimental study in dogs. Spine 1979;4:176-186.
DM
=
dura rnater; SC
=
spinal cord.
4. Gill GG, Scheck M. Kelley ET, Rodrigo JJ. Pedicle fat grafts for the prevention of scar in low-back surgery: A preliminary report on the first 92 cases. Spine 1985;10:662-667. 5. Trotter EJ. Thoracolumbar disc disease. In: Bojrab MJ, ed. Current TechniyucJsin Small Animal Surgery. 2nd ed. Philadelphia: Lea & Febiger, 1983:562-574. 6. Trotter EJ. Crissman J, Robson D, Babish J. Influence of nonbiologic implants on laminectorny membrane formation in dogs. Am J Vet Res 1988;49:634-643. 7. LaRocca H, Macnab I. The laminectomy membrane: Studies in its evolution, characteristics. effects and prophylaxis in dogs. J Bone Joint Surg 1974;56:545-550. 8. Brown NO, Helphrey ML. Prata RG. Thoracolumbar disc disease in the dog: A retrospective analysis of 187 cases. J A m Anim HOSPASSOC1977;13:665-672. 9. Prata RG. Neurosurgical treatment of thoracolumbar discs: The rationale and value of laminectomy with concomitant disc removal. J Am Anim Hosp Assoc 1981;17:17-26. 10. Jacobs RR, McClain 0, NeK J. Control of postlaminectomy Scar formation: An experimental and clinical study. Spine 19805:223229. 11. Chen PQ, Yang CY, Su CJ. Lee F. Prevention of postlaminectomy membrane: Experimental and clinical observations. Taiwan I Hsueh Tsa Chih 1989;88:57-61. 12. I(lviluoto 0. Use of free fat transplants to prevent epidural scar formation: An experimental study. Acta Orthop Scand Suppl 1976;( 164):3-75.
FAT GRAFTS AFTER LAMINECTOMY 13. Guigui P, Lassale B, Deburge A, et al. The value of polyglactin 910 in preventing peridural fibrosis and epiduro-arachnoiditis following laminectomy: Experimental study in rats. Rev Chir Orthop 1988;74:88-90. 14. Keller JT, Dunsker SB, McWhorter JM, et al. The fate of autogenous grafts to the spinal dura: An experimental study. J Neurosurg 1978;49:412-4 18. 15. Barber J, Gonzalez J, Esquerdo J, et al. Prophylaxis of the laminectomy membrane: An experimental study in dogs. J Neurosurg 1978;49:419-424. 16. Lee CK, Alexander H. Prevention of postlaminectomy scar formation. Spine 1984;9:305-3 12. 17. Mikawa Y, Hamagami H, Shikata J, et al. An experimental study on prevention of postlaminectomy scar formation by the use of new materials. Spine 1986;11:843-846. 18. Boot DA, Hughes SP. The prevention of adhesions after laminectomy: Adverse results of Zenoderm implantations into laminectomy sites in rabbits. Clin Orthop 1987;(215):296-302. 19. Van Akkerveeken PF, Van de Kraan W, Muller JW. The fate ofthe free fat graft: A prospective clinical study using CT scanning. Spine 1986;11:501-504. 20. Bryant MS, Bremer AM, Nguyen TQ. Autogeneic fat transplants in the epidural space in routine lumbar spine surgery. Neurosurgery 1983;13:367-370.
2 I . Saunders MC, Keller JT, Dunsker SB, Mayfield FH. Survival of autologous fat grafts in humans and in mice. Connect Tissue Res I98 1;8:85-91. 22. Mayer PJ, Jacobsen FS. Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft: A report of two cases. J Bone Joint Surg (Am) 1989;7 I : 1090-1093. 23. Deburge A, Bitan F, Lassale B, Vaquin G. Cauda equina syndrome caused by migration of a fat graft after laminoarthrectomy. Rev Chir Orthop 1988;74:677-678. 24. Prusick VR, Lint DS, Bruder WJ. Cauda equina syndrome as a complication of free epidural fat grafting: A report of two cases and a review of the literature. J Bone Joint Surg (Am) 1988;70: 1256- 1258. 25. Cabezudo JM, Lopez A, Bacci F. Symptomatic root compression by a free fat transplant after hemilaminectomy: Case report. J Neurosurg 1985;63:633-635. 26. Smith GK, Walter MC. Spinal decompressive procedures and dorsal compartment injuries: Comparative biomechanical study in canine cadavers. Am J Vet Res 1988;49:266-273. 27. Parker AJ, Smith CW. Functional recovery following incision of spinal meninges in dogs. Res Vet Sci 1972; I3:418-42 I. 28. Weisz GM, Gal A. Long-term survival of a free fat graft in the spinal canal: A 40-month postlaminectomy case report. Clin Orthop I986;(205):204-206.
Abstract of Current Literature EFFECTS OF CO2 LASER BEAM ON CORTICAL BONE Rayan GM, Pitha JV, Edwards JS, Everett RB Lasers in Surgery and Medicine 1991; 1 158-6 1 Sixteen bone blocks from two freshly amputated legs were used to study the effect of C02 laser on cortical bone. They were divided into two groups. In Group 1, the blocks were treated with C 0 2 laser using 1 mm spot (focused mode). In Group 2, they were treated with COz laser using 3 mm spot (defocused mode). Two other variables were investigated: the power and time of exposure. Three histologic zones were observed: a superficial zone with black particle deposits (carbonization), an intermediate zone with fibrillations and enlarged empty lacunae, and a deep zone with normal appearing bone. The bony changes in the first two zones combined were superficial in all specimens and did not exceed 200 microns. Increased energy, a focused beam, and time of exposure were all associated with increased matrix changes. C02 laser can be applied to cortical bone in vitro with minimal residual thermal damage.
Healing Characteristics of Free and Pedicle Fat Grafts after Dorsal Laminectomy and Durotomy in Dogs
Dorsal laminectomy and durotomy were performed at thoracic vertebrae 12 and 13 (T12-Tl3) and lumbar vertebrae 1 and 2 (Ll-L2) in 12 normal dogs. A free fat graft harvested from subcutaneous tissue adjacent to the incision was placed over the T12-T13 laminectomy site. A 75 X 25 x 5 mm pedicle fat graft harvestedfrom a similar location was placed over the LlL2 laminectomy site. Three dogs each were euthanatized at weeks 2, 4, 8, and 16. With both types of fat grafts, an initial inflammatory stage reduced the size of the graft approximately 50%. Axonal degeneration and demyelination of the spinal cord resolved by week 16. At week 16, the durotomy sites had healed, but the dura mater was adhered to the spinal cord. No difference between the grafts could be demonstrated by antemortern myelography and cerebrospinal fluid analysis. There was no demonstrable advantage to the use of pedicle fat grafts.
of a laminectomy is T formation of an epidural scar referred to as a laminectomy membrane. Excessive perineural fibrosis and HE INEVITABLECONSEQUENCE
scamng, dural adhesions, nerve root attenuation, and spinal cord compression and degeneration may complicate the healing process. The scar tissue may complicate surgical re-exploration of the laminectomy site. Nevertheless, such scar tissue formation is infrequently recognized as a clinical problem. Clinical manifestations of such complications are especially rare after heniilaminectomy; when present, they are usually associated with dorsal laminectomy procedures.I Many investigators have attempted to modify or to prevent formation of this scar tissue to avoid potential complications. Methods include modifications of surgical technique, pharmacologic manipulation of the healing process, and implantation of biologic and nonbiologic materials to separate the dura To from the raw surface of the paraspinal date, the most success appears to have been achieved with implantation of autogenous fat, either as a free fat graft or as a pedicle fat graft. It has been suggested that pedicle
grafts are superior to free grafts in preventing dural scar formation and bone closure over the laminectomy site and in protecting the spinal cord.24 The purpose of this investigation is to compare the healing characteristics of free and pedicle fat grafts placed over laminectomy and durotomy sites in dogs. Materials and Methods Two noncontiguous modified dorsal laminectomies (complete excision of the dorsal lamina and caudal articular processes, with excavation of the lateral laminae and pedicles) were performed in 12 mature, preconditioned beagle dogs.’ One laminectomy was centered over the junction of thoracic vertebrae 12 and 13 (T12-T 13) and one was centered over the junction of lumbar vertebrae I and 2 (Ll-L2). At each laminectomy site, a dorsal midline durotomy was performed. A free fat graft was harvested from the subcutaneous tissue dorsal to the deep fascia overlying the epaxial muscles and adjacent to the incision. Each graft was 5 to 7 mm thick, and each was
From the Departments of Small Animal Clinical Sciences (Trevor, Martin) and Pathobiology (Saunders), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, and the Department of Clinical Sciences (Trotter), New York State College of Veterinary Medicine, Ithaca, New York. Presented at the 20th Annual Meeting of the American College of Veterinary Surgeons, San Diego, California, February 1985. No reprints available.
282
TREVOR, MARTIN, SAUNDERS, AND TROTTER
283
Fig. 1. Fat grafts with dorsal laminectomy, week 2. Connective tissue septae are visible as narrow bands of white tissue coursing through the grafts. Distortion of the spinal cord is evident. Arrowheads delineate the fat grafts. (A) Free fat graft. (B)Pedicle fat graft.
trimmed to fill the bony defect created by the T I2-T 1 3 laminectom y. Pedicle fat grafts were created by sharply detaching subcutaneous fat along the margin of the incision, leaving the base attached caudally. The grafts were approximately 25 mm wide, 75 mm long, and 5 mm thick, with the length approximately three times the width of the base. The graft was placed directly over the spinal cord at the LI-L2 laminectomy site. In an attempt to avoid vascular compromise, the epaxial fascia adjacent to penetration of the pedicle graft was not closed. Mependine HCl (2.24.4 mg/kg) was administered as necessary to control postoperative pain. Three dogs each were euthanatized at weeks 2, 4, 8, and 16. Immediately before euthanasia, cerebrospinal fluid was collected by cisternal tap for Pandy test, cytologic evaluation including total and differential cell counts, and measurement of glucose, protein, pH, and specific gravity. Lumbar myelography was performed at the L4-L5 interspace. After necropsy, the vertebral column was removed intact from T10 to L4, dissected free of muscle, and frozen. While still frozen, transverse sections 1 cm thick were made with a band saw. The sections through disc spaces T11-Tl2, T12-Tl3, T13-L1, Ll-L2, and L2-L3 were thawed, fixed in 10% neutral buffered formalin, and decalcified. Prepared sections were stained with H & E and Masson’s tnchrome for collagen.
Results Eight dogs were nonambulatory (unable to support weight or walk with the hind limbs) immediately or within the first 72 hours after surgery. Four dogs remained ambulatory (capable of bearing weight and walking unassisted with hind limbs), but three were ataxic or had conscious propnoceptive deficits. All dogs euthanatized at weeks 2 and 4 were nonambulatory with diminished or no deep pain. At week 8, the six remaining dogs were walking, one with mild pelvic limb ataxia. The three dogs remaining at week 16 were walking normally. The results of the cerebrospinal fluid examinations were normal for all 12 dogs. Myelographic evidence of mild to severe spinal cord swelling, seen as vaned narrowing of the contrast columns, was present under six pedicle grafts and eight free grafts. Dorsal cord compression, identified by ventral deviation of the dorsal contrast column, was present under two pedicle grafts and two free grafts. Widening of the dorsal contrast column was present under one pedicle graft and one free graft. There was no consistent correlation between the nature or seventy of myelographic changes and the type of fat graft used to fill the laminectomy defect. At necropsy, pronounced dorsoventral compression of the spinal cord by both types of fat grafts was evident at week 2. At week 4, similar though less severe compression
FAT GRAFTS AFTER LAMINECTOMY
Fig. 2. Fat grafts with dorsal laminectomy, week 4. The fat is inflamed, with a mottled grey-and-white appearance. Arrowheads delineate the fat grafts. (A) Free fat graft. (B) Pedicle fat graft.
was evident. By week 8, the spinal cord had regained a more normal cross-sectional appearance, and at week 16 the shape of the spinal cord was normal. Grafts in both sites had shrunk 25% to 50% at week 2, and 50%by week 8. At week 16, each graft was about one-half its original thickness. Grey-white fat was identifiable, and fibrosis was evident as narrow bands of distinct white tissue coursing through the grafts. Foci of fat resorption and inflammation were visible as areas of yellow-brown discoloration within the grafts (Figs. 1-4). Histologically, inflammation, fat cell degeneration, and fibrosis were moderately severe at week 2. The inflammatory cell infiltrate consisted mainly of macrophages, lymphocytes, and plasma cells, with some scattered neutrophils. The neutrophils disappeared by week 4, by which time the fat degeneration and fibrosiswere more extensive. Associated with fat cell degeneration was formation of locules of free fat that appeared to induce a granulomatous response, including the formation of multinucleate giant cells. Severe inflammation, fat resorption, and fibrous tissue proliferation reached a peak in both grafts at week 8, and resolution of the inflammatory process and fat degeneration began (Fig. 5). In one dog euthanatized at week 8, there was only minimal inflammation in each graft. In two dogs, there was severe inflammation in the free fat
graft, but only mild change in the pedicle fat graft. By week 16, all inflammatory and degenerative changes had subsided in both grafts, leaving viable fat cells and a few delicate connective tissue septa (Fig 6). Significant inflammation was also evident adjacent to the grafts. At week 2, in the area previously occupied by the dorsal arch, numerous fragments of bone and suture were surrounded by a granulomatous response. This reaction subsided considerably by week 4, and was only occasionally present at week 8. The gap created in the dura mater filled in with fibrous connective tissue by week 2. In some locations involving both graft sites, this fibrosis was quite extensive and adhered to the dorsal surface of the spinal cord (Fig 7). The spinal cord at both graft sites suffered extensive axonal swelling and demyelination of all funiculi at week 2 (Fig. 8). Only mild changes were evident at week 4, and by week 8 they were nearly absent. No spinal cord abnormalities were present at week 16, but the dura mater, though rejoined, was still adherent to the spinal cord.
Discussion A multifactorial etiology has been proposed for laminectomy membrane formation, including factors such as
285
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 3. Fat grafts with dorsal laminectomy, week 8. Fat is visible. Spinal cord shows less distortion when compared with the 2-week group. Arrowheads delineate the fat grafts. (A) Free fat graft. (B) Pedicle fat graft.
length and location of the laminectomy site, hemostasis, height of remaining laminar bone, extent of epidural fat removal, and the type of implant interposed between the dura mater and paraspinal muscles.6 Laminectomy defects heal in a manner resembling endochondral bone formation arrested as a fibrous nonunion. Organization of the hematoma is followed by fibroblast invasion from the overlying epaxial muscles, resulting in fibrous callus formation and subsequent metaplasia to cartilage and sometimes b ~ n e . ~ Sequelae ,~.' include excessive cicatrix formation and epidural fibrosis, spinal dural scarring and adhesions, nerve root attenuation and entrapment, degeneration of the spinal cord, and stenosis of the spinal anal.^.^,' The scar tissue that forms may complicate re-exploration of the pine.^.^ Clinical manifestations of such complications, however, are infrequent. In a retrospective study of 187 dogs that underwent dorsal laminectomy and facetectomy, laminectomy membrane was a complication in only three dogs.* Modifications of surgical technique have been described, with smaller laminectomy defects and careful attention to hem0stasis.6,~In general, performing hemilaminectomies instead of laminectomies whenever possible has resulted in a lower incidence of clinical laminectomy membrane complications.I Nevertheless, dorsal laminectomy is preferred by some surgegns, especially for ventrally-situated disc herniations or when lateralization of
cord compression is not evident clinically or myelographically.',' Pharmacologic modification of the healing process with locally and parenterally administered pharmaceutic agents, including corticosteroids and hyaluronic acid, has been tried without S U C C ~ S S . ~ ~ ~ ~ ~ ~ - ' ~ Perhaps the best results have been achieved by interposing material to separate the spinal cord and dura mater from damaged paraspinal muscles. Nonbiologic materials that have been interposed include absorbable gelatin sponge, oxidized regenerated cellulose, absorbable gelatin film, micropore tape, methyl methacrylate, dacron, mylar, dimethyl siloxane polymer, polyethylene and other acrylic plastics, and polyglactin 9 R esults with these materials have been extremely varied and often less than optimal. Newer materials such as polylactic acid membrane and Elastase* have shown more p r o m i ~ e . ' ~ . ' ~ Biologic implants have also been investigated. k e l bone graft (contoured bovine bone) was found to be of some benefit in preventing invasion of scar tissue into the spinal canal." Porcine dermis treated to reduce its antigenic properties? did not prevent adhesions from forming after spinal surgery in rabbits." Autogenous fat grafts form an effective barrier, limiting scar extension into the spinal canal, decreasing scar tissue formation, and preventing 13'3-15
* Eisai Co. Ltd., Tokyo, Japan. t Zenoderm. Ethicon Ltd., Edinburgh. Scotland.
FAT GRAFTS AFTER LAMINECTOMY
Fig. 4. Fat grafts with dorsal laminectomy,week 16. Fat is normal in appearance, although reduced in size. No evidence of scar invasion into the spinal canal. In figure 4B, the pedicle of the fat graft is visible. Arrowheads delineate the fat grafts. (A) Free fat graft. (8)Pedicle fat graft.
dural adhesion^.^^'^^'^^^^ It has been suggested that the fat graft occupies a space that otherwise would become filled by hematoma.8Because it is flexible, the fat graft conforms to the margins of the laminectomy site, preventing leaks along which scar tissue might invade. Fat grafts avoid complications associated with stiffer nonbiologic materials, specifically problems with marginal fitting, implant displacement, and alteration of spinal biomechanics.6Fat grafts also reportedly avoid problems associated with flexible membranous nonbiologic materials, such as depression of the implant against the cord and subsequent dorsoventral flattening of the spinal canal.6 In this study, however, both free and pedicle fat grafts were responsible for severe dorsoventral cord compression that was apparent at week 2 and still evident at week 4.The neurologic status of these animals (nonambulatory paraparesis) and the histologic appearance of the spinal cord (axonal swelling and demyelination) were compatible with a compressive lesion. The cord compression may have been caused by the size (bulk) of the graft, postoperative inflammation and swelling of the fat graft, or closure of the epaxial fascia. Similar complications have been reported in Neurologic morbidity may have been higher in the dogs in this study than in clinical patients because the spine was destabilized by dorsal laminectomy in two locations rather than one, as is common in the clinical situation.26Nevertheless, it has been established that fat grafts are acceptable in clinical patients. It has
also been established that durotomy causes increased neurologic m~rbidity.~’ Reduction of the cord compression by weeks 8 and 16 probably resulted from resolution of the initial inflammation and swelling of the fat graft, decrease in the size of the fat graft by necrosis, and maturation of the granulation tissue into a more rigid connective tissue framework able to maintain cord shape. Although almost all remaining dogs in this study were clinically normal by weeks 8 and 16, care has to be taken to avoid compression of the spinal cord by the fat graft. In clinical patients, the symptoms of such compression may be confused with the symptoms of the transverse myelopathy for which the laminectomy procedure was performed. It has been recommended that a loop of 20or 22-gauge orthopedic wire be used to span the laminectomy defect. The wire is placed around the rostra1 and caudal spinal processes and moderately tightened, and the fascia and epaxial muscles are then sutured over the wire.’ This may aid in retaining a more normal architecture in the region of the laminectomy defect. To avoid excessive bulk that might compress the dura mater or nerve roots, the fat graft should be just large enough to cover the laminectomy defect and no more than 3 to 5 mm thick. Althou@ clinical success has been reported with thicker implants (10-1 5 rnm),l4 other investigators have obtained better results with grafts no thicker than 3 mm.3 During closure of the epaxial fascia, care should be
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 5. Severely inflamed free fat graft, week 8. Dense connective tissue can be seen infiltratingthe fat graft, surrounding the remaining foci of fatty tissue. H & E; x15. EM = epaxial musculature; FG = fat graft; SC = spinal cord.
287
Fig. 6. Free fat graft, week 16. There is complete resolution of the inflammation with normal fat. H & E; x15. FG = fat graft; DM = dura mater; SC = spinal cord.
between caudally based and cranially based flaps, or betaken to avoid forcing the fat graft and epaxial muscutween flaps brought over the midline and flaps tunneled lature onto the exposed spinal cord. through the adjacent mu~culature.~ In this study, 5 mm After implantation, a free fat graft goes through an inithick caudally based pedicle flaps were brought over the tial process involving necrosis of fat cells. Death of pormidline, taking care to avoid compression and vascular tions of the graft results in fat cyst formation, giant cell compromise of the pedicle by leaving the epaxial fascia formation, cellular infiltration, and f i b r o s i ~ . ~ , ~This , ' ~ . ~ ' adjacent to graft penetration unsutured. results in shrinkage of the fat graft to approximately onePedicle fat grafts are reported to be superior to free half its original s i ~ e . ~ .The ' ~ , remaining '~ implant survives grafts in preventing closure of bone over the laminectomy because of revascularization through a local blood supsite by preventing metaplasia of scar tissue to cartilage ply.3,'2.'4,2'928 Survival of a free fat graft is influenced by and bone.3 Fat cells of the pedicle grafts have been shown the amount of blood lost during the surgical procedure, to have improved survival with less cellular infiltration and fewer areas of fat necro~is.~ Pedicle fat grafts are rethe extent of surgical dissection, and the thickness of the portedly more effective than free fat grafts in preventing fat graft itself." dural scar formation and protecting the spinal cord against Several investigators have found pedicle fat grafts to be fibrosis and degenerative change^.^,^ Presumably, the superior to free fat In dogs, the deep fat derives its blood supply mainly from the deep f a ~ c i aFlaps . ~ with blood supply entering the fat graft through the attached a length-to-width ratio of 3: 1 and a thickness not greater pedicle maintains the viability of the graft, yielding superior results. than 3 mm were recommended. There was no difference
200
FAT GRAFTS AFTER LAMINECTOMY
Fig. 7. Free fat graft, week 2. The margins of the durotomy incision have scarred together and adhered to the spinal cord beneath. H 8 E; x20. FG = fat graft; DM = dura mater; SC = spinal cord.
The results of this study, however, indicated that the processes of healing and scar tissue formation were similar in both grafts. Each progressed through a severe granulomatous inflammation in response to fat degeneration, resulting in fibrosis and shrinkage of the graft, with the most extensive and severe changes 8 weeks after implantation. By week 16, the inflammatory process had resolved, leaving a viable fat graft reduced approximately 50% in size. In some cases, this shrinkage had become apparent as early as week 2. By week 16, the dura had rejoined but was adherent to the spinal cord. Histologically, there was no difference in healing of the durotomy sites. Extensive axonal degeneration and demyelination of the spinal cord at week 2, with resolution by week 16, was a reflection of the degree of cord compression. Myelographically and by gross inspection, no difference in cord compression could be demonstrated between graft types. In this study, no difference in healing properties or in the final outcome could be demonstrated between free and pedicle fat grafts.
There are several possible explanations for the similar results with both types of grafts in this study. No vascular studies were performed to define blood supply to the pedicle graft. This study mimicked clinical situationsin which the pedicle is based on paraspinal fat adjacent to the dorsal laminectomy site, not on a particular “axial pattern artery.” The laminectomy sites (T 12-T 13 and L 1-L2) are equally common sites of intervertebral disc protrusions treated by laminectomy. It is possible that the pedicle graft did not maintain circulation immediately after transposition. Consequently, both types of grafts may have been avascular from the beginning and thus may have had similar healing characteristics. Alternatively, the pedicle may have maintained perfusion to the graft, but neovascularization of the free graft may have occurred rapidly enough that by week 2 it was essentially complete; hence, healing of the two types of grafts was similar. Subjectively, there was no obvious difference in the amount of collagen (demonstrated with Masson’s trichrome stain) between the two grafts, indicating a similar inflammatory response.
289
TREVOR, MARTIN, SAUNDERS, AND TROTTER
Fig. 8. Free fat graft, week 2.There is axonal swelling and demyelination of the spinal cord. H 8 E; X75.
Since inflammation is a vascular event, this would imply similar vascularity. With either explanation, the similarity in healing indicates that there were no distinct advantages to the use of pedicle fat grafts in this study. Because of the ease and speed with which they can be harvested, our recommendation is to use free fat grafts with dorsal laminectomy. However, considerable care must be taken to avoid compression of the spinal cord by the fat graft. Furthermore, if adequate treatment can be provided by hemilaminectomy, then avoiding the dorsal laminectomy approach whenever possible is probably justified.
References I . Gage ED, Hoerlein BF. Hemilaminectomy and dorsal laminectorny for relieving compressions of the spinal cord in the dog. J Am Vet Med Assoc 1968;152:351-359. 2. Sakamoto K. Experimental study o n pedicle fat grafts after faminectomy: Comparison of pedicle fat and free fat grafts. Nippon Seikeigeka Gakkai Zasshi 1987;61:743-753. 3. Gill GG, Sakovich L, Thompson E. Pedicle fat grafts for the prevention of scar formation after laminectomy: An experimental study in dogs. Spine 1979;4:176-186.
DM
=
dura rnater; SC
=
spinal cord.
4. Gill GG, Scheck M. Kelley ET, Rodrigo JJ. Pedicle fat grafts for the prevention of scar in low-back surgery: A preliminary report on the first 92 cases. Spine 1985;10:662-667. 5. Trotter EJ. Thoracolumbar disc disease. In: Bojrab MJ, ed. Current TechniyucJsin Small Animal Surgery. 2nd ed. Philadelphia: Lea & Febiger, 1983:562-574. 6. Trotter EJ. Crissman J, Robson D, Babish J. Influence of nonbiologic implants on laminectorny membrane formation in dogs. Am J Vet Res 1988;49:634-643. 7. LaRocca H, Macnab I. The laminectomy membrane: Studies in its evolution, characteristics. effects and prophylaxis in dogs. J Bone Joint Surg 1974;56:545-550. 8. Brown NO, Helphrey ML. Prata RG. Thoracolumbar disc disease in the dog: A retrospective analysis of 187 cases. J A m Anim HOSPASSOC1977;13:665-672. 9. Prata RG. Neurosurgical treatment of thoracolumbar discs: The rationale and value of laminectomy with concomitant disc removal. J Am Anim Hosp Assoc 1981;17:17-26. 10. Jacobs RR, McClain 0, NeK J. Control of postlaminectomy Scar formation: An experimental and clinical study. Spine 19805:223229. 11. Chen PQ, Yang CY, Su CJ. Lee F. Prevention of postlaminectomy membrane: Experimental and clinical observations. Taiwan I Hsueh Tsa Chih 1989;88:57-61. 12. I(lviluoto 0. Use of free fat transplants to prevent epidural scar formation: An experimental study. Acta Orthop Scand Suppl 1976;( 164):3-75.
FAT GRAFTS AFTER LAMINECTOMY 13. Guigui P, Lassale B, Deburge A, et al. The value of polyglactin 910 in preventing peridural fibrosis and epiduro-arachnoiditis following laminectomy: Experimental study in rats. Rev Chir Orthop 1988;74:88-90. 14. Keller JT, Dunsker SB, McWhorter JM, et al. The fate of autogenous grafts to the spinal dura: An experimental study. J Neurosurg 1978;49:412-4 18. 15. Barber J, Gonzalez J, Esquerdo J, et al. Prophylaxis of the laminectomy membrane: An experimental study in dogs. J Neurosurg 1978;49:419-424. 16. Lee CK, Alexander H. Prevention of postlaminectomy scar formation. Spine 1984;9:305-3 12. 17. Mikawa Y, Hamagami H, Shikata J, et al. An experimental study on prevention of postlaminectomy scar formation by the use of new materials. Spine 1986;11:843-846. 18. Boot DA, Hughes SP. The prevention of adhesions after laminectomy: Adverse results of Zenoderm implantations into laminectomy sites in rabbits. Clin Orthop 1987;(215):296-302. 19. Van Akkerveeken PF, Van de Kraan W, Muller JW. The fate ofthe free fat graft: A prospective clinical study using CT scanning. Spine 1986;11:501-504. 20. Bryant MS, Bremer AM, Nguyen TQ. Autogeneic fat transplants in the epidural space in routine lumbar spine surgery. Neurosurgery 1983;13:367-370.
2 I . Saunders MC, Keller JT, Dunsker SB, Mayfield FH. Survival of autologous fat grafts in humans and in mice. Connect Tissue Res I98 1;8:85-91. 22. Mayer PJ, Jacobsen FS. Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft: A report of two cases. J Bone Joint Surg (Am) 1989;7 I : 1090-1093. 23. Deburge A, Bitan F, Lassale B, Vaquin G. Cauda equina syndrome caused by migration of a fat graft after laminoarthrectomy. Rev Chir Orthop 1988;74:677-678. 24. Prusick VR, Lint DS, Bruder WJ. Cauda equina syndrome as a complication of free epidural fat grafting: A report of two cases and a review of the literature. J Bone Joint Surg (Am) 1988;70: 1256- 1258. 25. Cabezudo JM, Lopez A, Bacci F. Symptomatic root compression by a free fat transplant after hemilaminectomy: Case report. J Neurosurg 1985;63:633-635. 26. Smith GK, Walter MC. Spinal decompressive procedures and dorsal compartment injuries: Comparative biomechanical study in canine cadavers. Am J Vet Res 1988;49:266-273. 27. Parker AJ, Smith CW. Functional recovery following incision of spinal meninges in dogs. Res Vet Sci 1972; I3:418-42 I. 28. Weisz GM, Gal A. Long-term survival of a free fat graft in the spinal canal: A 40-month postlaminectomy case report. Clin Orthop I986;(205):204-206.
Abstract of Current Literature EFFECTS OF CO2 LASER BEAM ON CORTICAL BONE Rayan GM, Pitha JV, Edwards JS, Everett RB Lasers in Surgery and Medicine 1991; 1 158-6 1 Sixteen bone blocks from two freshly amputated legs were used to study the effect of C02 laser on cortical bone. They were divided into two groups. In Group 1, the blocks were treated with C 0 2 laser using 1 mm spot (focused mode). In Group 2, they were treated with COz laser using 3 mm spot (defocused mode). Two other variables were investigated: the power and time of exposure. Three histologic zones were observed: a superficial zone with black particle deposits (carbonization), an intermediate zone with fibrillations and enlarged empty lacunae, and a deep zone with normal appearing bone. The bony changes in the first two zones combined were superficial in all specimens and did not exceed 200 microns. Increased energy, a focused beam, and time of exposure were all associated with increased matrix changes. C02 laser can be applied to cortical bone in vitro with minimal residual thermal damage.
